1. Field of the Invention
The present invention relates to the field of diagnosis and treatment of perceptual impairments, and in particular, relates to the treatment of reading-related or dyslexic impairments which are visual disturbances heretofore having an undiagnosed cause.
2. Description of the Prior Art
There are many perceptual impairments, particularly relating to learning disabilities, the causes of which are not understood. These impairments are symptomatically evidenced in a variety of ways which do not lead to a logically discernible categorization. These impairments or symptoms are referred to as dyslexia, which is loosely defined to include any impairment of the ability to read due to a brain defect.
Dyslexic impairments in children and adults substantially interfere with the patient's ability to adapt to conventional, formal education, and have far-reaching, lifelong social and economic implications for the patient.
The current treatment of dyslexia and related learning disabilities, as well as other forms of learning underachievement, are treated by a multi-disciplinary approach, from the arts of medicine, education, and psychology. Since dyslexia is currently believed to be a structural brain defect, as confirmed by a prior universal failure to derive any symptomatic relief for dyslexic patients through ocular treatment, the present state of treatment is directed to the central nervous system and brain. Ocular treatment is not expected, according to prior art experience, to have any effect on the brain's processing of visual stimuli. See, for example, American Academy of Ophthalmology Policy Statements, Ophthalmology Times, January 1982, at page 8-11.
The reason for this prior art belief is that children with dyslexia or related learning disabilities are observed to have the same incidence of ocular abnormalities, for example, refractive errors and muscle imbalance, including near-point convergence and binocular fusion deficiencies, as children without dyslexia. There is also no known peripheral eye defect that produces dyslexia and associated learning disabilities. Eye defects further do not cause reversal of letters, words or numbers. Recent studies suggest that dyslexia and associated learning disabilities may be related to genetic, biochemical, and/or structural brain changes. See, for example, University of Miami, "Chromosome 15 May Cause Dyslexia", Medical World News, Dec. 2, 1980, at p. 24; Shaywitz, et al., "The Biochemical Basis of Minimal Brain Dysfunction", Journal of Pediatrics 2:179-187, 1978.
According to the present state of the art, no known evidence supports any claim for improving the academic abilities of dyslexic or learning disabled children, or modifying delinquent or criminal behavior with treatment based on visual training, including: muscular exercises; ocular pursuit; tracking exercises; glasses (with or without prisms); neurologic organizational training, including laterality training and balance board; or perceptual training. Excluding correctable ocular defects, glasses (with or without prisms) have thus far been found to have no value in the specific treatment of dyslexia or any related learning disability.
Therefore, what is needed is a method of diagnosis and treatment which can assist in symptomatically treating and correcting the perceptual impairments that are suffered by dyslexic patients.